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         SCIENTIFIC PROOF OF CHRONIC LYME

NONE of the work on this page is mine. I have provided direct links to the original work. If this work is from your site and you do not want it displayed here please email me and I will remove it immediately. b10g7@verizon.net

 

FROM:  

Cheryl's Lyme Info .Net Website Lyme Files

SPECIAL COMPILATIONS OF SCIENTIFIC ABSTRACTS:
The following files were developed by a Lyme patient, and are provided here with permission. They require Adobe Acrobat which, if not already on your computer, can be downloaded for free at: adobe.com If you have acrobat reader, but still experience difficulty viewing the files, see "Enabling the Browser" 

http://www.lymeinfo.net/LDPersist.pdf and
http://www.lymeinfo.net/lymefiles.html#sci

 

From: http://www.lymealliance.org/research/grier/grier_5.php

Chronic Lyme Post-Mortem Study Needed

Editorial by Tom Grier:

SNIPPED to references:

  • Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from joint fluid three months after treatment of facial palsy due to Lyme Borreliosis. J Infect Dis 1988;158:905-906
  • Liegner KB, Shapiro JR, Ramsey D, Halperin AJ, Hogrefe W, and Kong L. Recurrent erythema migrans despite extended antibiotic treatment with minocycline in a patient with persisting Borrelia burgdorferi infection. J. American Acad Dermatol. 1993;28:312-314
  • Waniek C, Prohovnik I, Kaufman MA. Rapid progressive frontal type dementia and death with subcortical degeneration associated with Lyme disease. A biopsy confirmed presence of Borrelia burgdorferi post-mortem. A case report/abstract/poster presentation. LDF state of the art conference with emphasis on neurological Lyme. April 1994, Stamford, CT*
  • Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic Relapsing Neuroborreliosis. European Neurology. 1995;35(2):113-117
  • Cleveland CP, Dennler PS, Durray PH. Recurrence of Lyme disease presenting as a chest wall mass: Borrelia burgdorferi was present despite five months of IV ceftriaxone 2g, and three months of oral cefixime 400 mg BID. The presence of Borrelia burgdorferi confirmed by biopsy and culture. Poster presentation LDF International Conference on Lyme Disease research, Stamford, CT, April 1992 *
  • Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U, Kalden JR and Burmester GR: Persistence of Borrelia burgdorferi in ligamentous tissue from a patient with chronic Lyme Borreliosis. Arthritis and Rheum 1993;36:1621-1626
  • Lavoie Paul E MD. Protocol from Rakel's: Explains persistence of infection despite "standard" courses of antibiotics. Lyme Times-Lyme Disease Resource Center 1992;2(2): 25-27 Reprinted from Conn's Current Therapy 1991
  • Masters EJ, Lynxwiler P, Rawlings J. Spirochetemia after continuous high dose oral amoxicillin therapy. Infect Dis Clin Practice 1994;3:207-208
  • Pal GS, Baker JT, Wright DJM. Penicillin resistant Borrelia encephalitis responding to cefotaxime. Lancet I (1988) 50-51
  • Preac-Mursic V, Wilske B, Schierz G, et al. Repeated isolation of spirochetes from the cerebrospinal fluid of a patient with meningoradiculitis Bannwarth' Syndrome. Eur J Clin Microbiol 1984;3:564-565
  • Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A, and Prokop J. Survival of Borrelia burgdorferi in antibiotically treated patients with Lyme Borreliosis Infection 1989;17:335-339
  • Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J. Infect Dis 1992;166:440-444
  • Haupl TH, Krause A, Bittig M. Persistence of Borrelia burgdorferi in chronic Lyme Disease: altered immune regulation or evasion into immunologically privileged sites? Abstract 149 Fifth International Conference on Lyme Borreliosis, Arlington, VA, 1992 *
  • Lavoie Paul E. Failure of published antibiotic regimens in Lyme borreliosis: Observations on prolonged oral therapy. Abstract presented at the 1990 Lyme Borreliosis International Conference in Sweden.*
  • Fried Martin D, Durray P. Gastrointestinal Disease in Children with Persistent Lyme Disease: Spirochetes isolated from the G.I. tract . 1996 LDF Lyme Conference Boston, MA, Abstract*
  • Neuroboreliosis: In the journal Annals of Neurology Vol. 38, No 4, 1995, there was a brief article by Dr. Andrew Pachner MD, Elizabeth Delaney BS, and Tim O'Neill DVM, Ph.D. The conclusion of the article was simple and concise: " These data suggest that Lyme neuroboreliosis represents persistent infection with B. burgdorferi." The study used nonhuman primates as a model for human neuroborreliosis, and used a special PCR technique to detect the presence of Borrelia DNA within specific structures of the brains of five rhesus monkeys. The monkeys were injected with strain N40Br of Borrelia burgdorferi, and later autopsied for analysis.

From: http://www.centurytel.net/tjs11/bug/blot1.htm#n6

"These data suggest that LYME NEUROBORELIOSIS REPRESENTS PERSISTENT INFECTION WITH b. BURGDORFERI."

The study used nonhuman primates as a model for human neuroborreliosis, and used a special PCR technique to detect the presence of Borrelia DNA within specific structures of the brains of five rhesus monkeys. The monkeys were injected with strain N40Br of Borrelia burgdorferi, and later autopsied for analysis.

ABSTRACT SUMMARIES:

  • Abstract # D654 - J. Nowakowski, et al. Culture-Confirmed Treatment Failures of Cephalexin Therapy for Erythema Migrans. Two of six patients biopsied had culture confirmed Borrelia burgdorferi infections despite up to 21 days of cephalexin (500 mg TID) antibiotic treatment.
  • Abstract # D655 - Nowakowski, et al, Culture-confirmed infection and reinfection with Borrelia burgdorferi. A patient, despite antibiotic therapy, had a recurring Erythema Migrans rash on three separate occasions. On each occasion it was biopsied, which revealed the active presence of Borrelia burgdorferi on two separate occasions, indicating reinfection had occurred.
  • Abstract # D657 - J. Cimperman, F. Strle, et al, Repeated Isolation of Borrelia burgdorferi from the cerebrospinal fluid (CSF) of two patients treated for Lyme neuroborreliosis.

    Patient One was a twenty year old woman who presented with meningitis but was seronegative for Borrelia burgdorferi. Subsequently, six weeks later

    Bb was cultured from her CSF and she was treated with IV Rocephin 2 grams a day for 14 days. Three months later, the symptoms returned and Bb was once again isolated from the CSF.

    Patient 2 was a 51 year old female who developed an EM rash after tick bite. Within two months she had severe neurological symptoms. Her serology was negative. She was denied treatment until her CSF was culture positive nine months post-tick bite.

    She was treated with 2 grams of Rocephin for 14 days. Two months post-antibiotic treatment, Bb was once again cultured from her CSF.

    In both of these cases, the patients had negative antibodies but were culture positive, suggesting that the antibody tests are not reliable predictors of neurological Lyme Disease. Also, standard treatment regimens are insufficient when infection of the CNS is established and Bb can survive in the brain despite intravenous antibiotic treatment.

  • Patients with ACA shed Bb DNA post treatment: Aberer E, et al. Success and Failure in the treatment of Acrodermatitis Chronica Atrophicans (ACA) skin rash. Infection 24(1):85-87 1996.

    ACA is a late stage skin rash usually attributed to Borrelia afzelii, it is sometimes mistaken for scleroderma.

    Forty-six patients with ACA were treated with either 14 days of IV Rocephin or thirty days of oral penicillin or doxycycline and followed up for one year. Of those treated with IV, 28% had no improvement, and 40% still shed Bb antigen in their urine. Of the oral group, 70% required retreatment. Conclusion: Proper length of treatment for ACA has yet to be determined.

  • Logigian EL, McHugh GL, Antibiotics for Early Lyme Disease May Prevent Full Seroconversion but not CNS Infection. 1997 ABSTRACT # S66.006 Neuloogy Symposia, NEUROLOGY 1997; A388:48.

    In this study, 22 late-stage neurological patients who met the Centers for Disease Control (CDC) criteria for Lyme disease were studied over a three year period.

    Eighty-five percent of seronegative patients who still had active disseminated infection had been treated within one month of tick bite. This means that early antibiotic treatment may make you test negative, but you still progress to develop encephalitis.

    Without antibodies your brain has no natural immunity or local immune system to fight the infection, so WITHDRAWING ANTIBIOTICS CAUSES THE INFECTION IN THE CENTRAL NERVOUS SYSTEM (CNS) TO GO UNABATED. Patients who go on to develop brain infections despite antibiotics, may have suppressed antibody production thus worsening any remaing active infection in the Central Nervous System.

  • Arthritis: A three year follow-up: Valesova H, Mailer J, et al. Long-term results in patients with Lyme disease followed for three years after two weeks of IV Rocephin. Infection 24(1):98-102, 1996.

    This study represents another of the problems with author's bias interpretation of data. Thirty-five Lyme arthritis patients were treated with a two week course of IV Rocephin. They were then followed for three years.

    At the end of the study, six patients had complete relapses, nineteen had marked improvement, four had new Lyme symptoms, and the rest were lost to follow up. The authors conclusion: " The treatment results for this group of 35 Lyme arthritis patients are considered successful."

    Let's look at the figures more closely; Out of a total of 29 patients out of 35 that were contacted post treatment: 19 improved = 65% 6 relapsed = 20 % 4 worsened = 15 % Does a total of 35% of patients still suffering sound like successful treatment to you?

    This is a treatable disease, but you have to treat it! What if a doctor's child was one of the 35%? Do you think they would continue go untreated as suggested by the ACP? How many patients have to relapse before treatment is considered unsuccessful? Six patients or 20% had complete relapses yet the conclusion of the study was that in general treatment was considered successful!

    We get better cure rates for Tuberculosis!

    Animal vs. Human Studies: Support for the theory that BORRELIA BURGDORFERI CAN FIND SAFE HAVENS IN SEQUESTERED SITES despite antibiotic therapy comes from several animal model studies.

    However, only a few human cases have yet been published. This is because the tissue studies that are required almost demand that they be done in a post-mortem exam. (See Stanek and Appel's work on skin biopsies versus post-mortem exam of deep tissues in Lyme infected and antibiotic treated beagles)

  • Abstract # D607 - M.J.G. Appel, The persistence of Bb in Dogs after antibiotic treatment. Seventeen Beagle puppies were infected with Bb from infected ticks, eleven were treated for four weeks with either Doxycycline or amoxicillin in doses according to weight. Six were control dogs. 1/11 had Bb isolated from skin, but 7/11 dogs had Bb isolated from other tissues during post-mortem.

    All of the persistent infected pups had persistent arthritis. Conclusion: Skin biopsies are not predictive of persistence of infection. Also the standard excepted four week course of antibiotic treatment in dogs is not sufficient.

    To date, no major multi-center post-mortem Lyme disease study has ever been done on humans. Without this type of post-mortem study, the debate between the two disagreeing camps will almost certainly continue.

    Results from the European Alzheimers study done by Dr. Judit Miklossy suggests that post-mortem exams should not only look for persisting spirochetes in deceased Lyme patients, but should also look for spirochetes in the brains of deceased dementia patients as well.

  • Miklossy Judit. Alzheimer's disease a spirochetosis? Neuro Report 1993;4:841-848o

    Thirteen out of thirteen Alzheimer patients had spirochetes in the brain. None of the age-matched control subjects had evidence of spirochetes in their brains.

    This study suggests that there is a correlation between an Alzheimer's dementia and CNS spirochetosis in Swiss patients. In other words spirochetes might contribute to a CNS dementia similar to Alzheimer's disease.

    This is not to suggest that all Alzheimer's is caused by spirochetes, but even if a small percentage of dementia can be prevented by antibiotics then further studies are justified. None are currently being done!

  • Miklossy J, Kuntzer T, Bogousslavsky J, et al. Meningovascular form of neuroborreliosis: Similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary Neurosyphilis. Acta Neuro Pathol 1990;80:568-572
  • [AUTHORS: Jobe DA; Rawal N; Schell RF; Callister SM

    TITLE: Detection of borreliacidal antibodies in Lyme borreliosis patient sera containing antimicrobial agents.

    AUTHOR AFFILIATION: Microbiology Research Laboratory, Gundersen Lutheran Medical Center, La Crosse, Wisconsin 54601, USA.

    SOURCE: Clin Diagn Lab Immunol 1999 Nov;6(6):930-3

    CITATION IDS: PMID: 10548588 UI: 20018406

    ABSTRACT: The borreliacidal-antibody test has been used for the serological detection and confirmation of Lyme borreliosis. However, the presence of antimicrobial agents in serum can confound the accurate detection of borreliacidal antibodies.

    In this study, we developed a Bacillus subtilis agar diffusion bioassay to detect small concentrations of antimicrobial agents in serum.

    We also used XAD-16, a nonionic polymeric resin, to adsorb and remove high concentrations of amoxicillin, cefotaxime, ceftriaxone, cefuroxime, doxycycline, and erythromycin without significantly affecting even small concentrations of immunoglobulin M (IgM) or IgG borreliacidal antibodies.

    High concentrations of penicillin could also be removed by adding 1 U of penicillinase without significantly influencing the levels of borreliacidal antibodies. These simple procedures greatly enhance the clinical utility of the borreliacidal-antibody test.]

To do these kind of tissue studies of sequestered spirochetal infections takes nearly heroic efforts in time, costs, and diligence. Yet the few times that these types of studies have been applied to humans have suggested that Borrelia burgdorferi can indeed survive and thrive within the human body despite a complete course - or even several courses - of antibiotic therapy.

Camp A maintains that Lyme disease is relatively easy to diagnose by means of serology and is easily cured with antibiotics. So it follows that any study proving active infection post-antibiotics would disprove their position.

Yet despite several such studies and case histories, Camp A still maintains that persistence of symptoms post-antibiotic treatment of Lyme disease is not due to persistence of infection.

Why? How can they maintain this position if it has been repeatedly disproved?